Apomorphine-induced yawning in rats is abolished by bilateral 6-hydroxydopamine lesions of the substantia nigra

Abstract

Apomorphine-induced yawning was studied in male rats with bilateral 6-hydroxydopamine lesions of the substantia nigra. Apomorphine 10, 20 and 50 micrograms/kg SC induced dose-dependent yawning in unoperated controls and animals with sham lesions. In the lesioned animals (in which the mean striatal dopamine depletion was 67%), the maximum yawning response rate was greatly attenuated with no evidence that the dose response curve was shifted in either direction. Furthermore, blockade of yawning in the lesioned animals was not simply due to suppression by other stereotyped behaviours, since there was no evidence of increased sniffing or chewing in these animals. These data provide further support for the hypothesis that apomorphine-induced yawning is mediated by dopamine autoreceptors and requires intact nigrostriatal projections.

Acute buspirone abolishes the expression of behavioral dopaminergic supersensitivity in mice

“…Specifically, since buspirone seems to block preferentially presynaptic dopamine receptors as compared to the postsynaptic ones (19), it was suggested that the ability of chronic buspirone treatment to attenuate the development of behavioral supersensitivity could be related to the development of presynaptic dopamine receptor supersensitivity (leading to a decreased availability of dopamine in the synaptic cleft). In line with this possibility, while Tunnicliff et al (20) showed that withdrawal from repeated treatment with buspirone led to marked reductions in the synthesis of dopamine in the rat striatum, we have shown that the drug potentiates yawning behavior induced by small doses of apomorphine (16), which is considered a behavioral parameter of nigrostriatal dopaminergic presynaptic function (21). In addition, we have demonstrated that withdrawal from longterm haloperidol treatment at doses that selectively block dopamine autoreceptors decreases open-field behavior, suggesting that the development of dopamine autoreceptor supersensitivity can attenuate the behavioral effects produced by postsynaptic dopamine receptor supersensitivity (22).…”

The effects of dihydropyridine compounds in behavioural tests of dopaminergic activity

“…Although apomorphine-induced yawning was potentiated by nifedipine and inhibited by Bay K 8644, penile erection induced by the same compound, and both the stimulus effects of amphetamine and the rotational behaviour induced by amphetamine were unaffected by either compound. Apomorphine-induced yawning is thought to be the result of reduced dopamine release following stimulation of presynaptic dopamine receptors (Mogilnicka & Klimek, 1977;Protais et al, 1983;Gower et al, 1984;Stahle & Ungerstedt, 1984;Stoessl et al, 1987) (Gower et al, 1984) and the inability of the dihydropyridine compounds to affect this parameter argues against an interaction with either apomorphine itself or dopamine release mechanisms. This conclusion is further supported by the lack of effect of either nifedipine or Bay K 8644 on amphetamine drug discrimination and on rotation in unilaterally lesioned rats, either alone or in combination with amphetamine.…”

Do autoreceptors mediate dopamine agonist — induced yawning and suppression of exploration? A critical review

“…Other results supporting the autoreceptor hypothesis are that lesions of the striatum (Dourish and Hutson 1985) or the substantia nigra by 6-OHDA (Stoessel et al 1987) or in the substantia nigra by electrocoagulation (Maj et al 1977) abolish yawning induced by APO given systemically. However, Scheel-Krtiger (1986) found that yawning, induced by local injection of DA agonists into the striatum, was not abolished by 6-OHDA lesions in the same region.…”